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Pembahasan LO 12-8-2013 & 19-8-2013

1. Gastropathy portal hypertension


Gastropathy Portal Hypertension
Definisi: Gastric vascular changes associated with portal hypertension.
Etiologi: sebagai komplikasi dari portal hypertension baik yang disebabkan
oleh sirosis atau pun yang non sirosis.
Pathogenesis : Belum diketahui dengan jelas dan pasti tetapi ada
beberapa hypothesis yang mungkin berkaian:
Elevated portal pressure.
Some other humoral factors (increased circulating levels of
vasodilators such as gluca- gon, or a reduced sensitivity to
endogenous vasoconstrictors may play a significant role. This
hypothesis was sup- ported by the fact that the levels of several
vasodilators including glucagon, norepinephrine, VIP, gastrin or
secretin, were found to be increased in the plasma of cirrhotic portal
hypertensive patients and/or animals).
Several endothelial factors including prostagladins, NO and vascular
endothelial growth factor.
Lokasi: in the gastric fundus and upper body of the stomach although it
can affect the whole stomach and even other areas of the gastrointestinal
tract, such as the small bowel or the colon.
Gambaran klinis: overt or chronic upper gastrointestinal bleeding, chronic
gastric mucosal bleeding and recurrent iron deficiency anemia that
sometimes requiring blood transfusion.
Endoscopic finding classification:

Histological features:
Dilatation of the capillaries and collecting venules in the gastric
mucosa.
Submucosal veins appear ectatic, ir- regular and with areas of intimal
thickening.
A greater mean mucosal capillary cross-sectional area.
Absence of any significant inflammatory cell infiltrate or erosion of the
gastricmucosa.
Severe PHG : the number of mucosal vessels exhibiting fibrin thrombi and
ectasia and spindle cell proliferation [smooth muscle cell and myofibroblast
hyperplasia] in the superficial mucosa are greater.
Tatalaksana :
Beta adrenergic blockers (propanolol), addition of isosorbite 5-mononi-
trate to propanolol if not efficient
Intravenous infusion of vasopressin
Glypressin or somatostatin
Endoscopic photocoagulation or electrocoagulation
Endoscopic photocoagulation or electrocoagulation
Decompressive shunt surgery
TIPSS.
DD : GAVE (Gastric Antral Vascular Ectasia)


2. Hubungan sirosis dengan gastric ulcer
Increased resistance to portal blood flow in patients with liver disease (with
and without cirrhosis) and the consequent elevation in portal pressure.
Chronic endotoxemia; the mechanism of susceptibility to mucosal injury is
thought to be related to an imbalance between gastric mucosal aggressive
and defensive factors.
The ability of the gastric mucosa to repair itself following injury is also
compromised in these individuals.
Reduced delivery of oxygen to the gastric mucosa, a phenomenon related to
the modi- fied tissue architecture (vascular congestion) and blood flow
regulation of the stomach and lungs in portal hypertension, has a role in the
reduced resistance of gastric mucosa to irri- tants in patients with cirrhosis
and portal hypertension.
Reduced basal or stimulated gastric acid secretion, a phenomenon probably
secondary to a compensatory adaptation to cirrhosis and portal hypertension.
An increase in gastric blood flow in response to the presence of acid or
irritants on the mucosa enables neutralization of toxins or noxious agents and
is termed the gastric hyperemic response. Reduced responsive- ness of the
gastric microcirculation to injury is believed to be associated with diminished
gastric prostaglandin production, a phenom- enon related to the significantly
increased nitric oxide production and release associated with the
hyperdynamic circulation seen in portal hypertension.
Acute or chronic administration of the prostaglandin analog misoprostol
restores the responsiveness of the rat gastric microcirculation to acid and
ethanol as well as to nitric oxidea critical downstream mediator of the
gastric hyperemic response to irritants.

3. Bedanya Psychosomatic dan Psychiatric
Psychosomatic = suatu kondisi terjadinya stress ataupun gangguan mental
yang menyebabkan timbulnya suatu gejala fisik (seperti migraine, tension
headaches, sexual dysfunction, hypertension , dan gastrointestinal problems)
yang tidak berhubungan dengan suatu penyakit fisiologis.
Psychiatric = suatu kondisi yang terjadi akibat gangguan ataupun stress
mental tanpa menimbulkan berbagai gejala fisik.

4. ESR yang signifikan untuk pasien TBC = >100 mm/hour
(http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=sho
w_test&id=249&Itemid=34)
Normal Results
Adults (Westergren method):
Men under 50 years old: less than 15 mm/hr
Men over 50 years old: less than 20 mm/hr
Women under 50 years old: less than 20 mm/hr
Women over 50 years old: less than 30 mm/hr
Children (Westergren method):
Newborn: 0 to 2 mm/hr
Newborn to puberty: 3 to 13 mm/hr
(http://health.nytimes.com/health/guides/test/esr)
5. Rasio albumin globulin normal dan pada pasien sirosis
Normal range of albumin = 3.9 to 5.1 g/dL. Normal range of globulins
= 2.3 to 3.5 g/dL.
(http://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeI
D=167&ContentID=total_protein_ag_ratio)
Rasio Albumin/Globulin normal =1.2 - 1.5
(http://www.ecopolitan.com/health-services/specific-health-conditions/291-
blood-interpretation?start=27)
Rasio Albumin/Globulin pada pasien Sirosis = 1
(http://www.ncbi.nlm.nih.gov/pubmed/11995477)
6. Renal and liver problems apa saja yang terdapat prolonged fever?
PROLONGED FEVER IN LIVER PROBLEMS
Occurrence of fever in a patient with liver problems should suggest the
following:
1. Hepatoma ( HCC )- hepatocellular carcinoma , presenting low grade fever
because of poor liver function with increase proinflammantory cytokines and
chemokines
2. Liver cirrhosis and hepatitis : Endotoxemia. Endotoxins are normally
present in portal blood; in hepatic cirrhosis they are insufficiently cleared by
the liver and their presence can be demonstrated in the systemic circulation.
Fever is one of the many consequences ascribed to the presence of
endotoxins in the blood with low grade fever. In cirrhosis / chronic liver
disease gradual destruction of liver tissue trigger proinflammantory
response.
3. Cholecystitis gall stone stuck
in the cystic duct and in late terms
causes infection in hepatic duct.
infection in bile duct
cholangits(septicaemia), sistemic infection
and fever.

PROLONGED FEVER IN KIDNEY
PROBLEMS
Low grade fever is commonly seen in kidney disease. When it occurs, the
patients are usually suspected to have infections. Due to the following causes,
the patients with kidney disease are more likely to have infections like urinary
tract infection, upper
respiratory tract
infection.
The patients with
kidney disease
usually have to
depend on long
term use of
immunosuppressive
agents. These
medications not only
suppress the
inflammatory
response in kidneys,
but also weaken
immune system.
Thus, the patients
are susceptible to
develop infection.
Proteins are
antibodies in our
body and they can defeat virus, bacteria when they invade into body.
However, in some cases of kidney diseases, the patients may lose a large
amount of proteins in urine. As a result, the patients immunity will decline and
bacteria and virus will invade into body.
The above are the main causes of infection in kidney disease. When it occurs,
the patients may experience low grade fever. If urinary tract infection occurs,
urgent urination, painful urination etc also can occur.
Therefore, if you have low grade fever, you should go to see a doctor at once
to find out if it is related to infection. Meanwhile, the patients should also take
preventive measures to reduce the risk of infection.
1. Chronic kidney failure / end stage renal disease such as cause
pyelonephritis chronic, renal abcess, hydronephrosis and etc. Low
grade fever happens because poor immunity, long term application of
immunosuppressive agents and loss of usefull protein in urine.
2. Acute kidney failure high inflammantory response occurs such as
sepsis because of bad ascending infection, dehydration, damage from
long term effect some
medicine(gentamicin,streptomycin,aspirin,ibuprofen,ACE inhibitors),
kidney stones, kidney injury cause trauma and etc.
Kidney cancer ( wilms tumor / renal cell carcinoma ) Produce
proinflammantory cytokines.
7. Fever of unknown origin : Fever that lasts 3 weeks or longer with
temperatures exceeding 100.9F with no clear diagnosis despite 1 week of
clinical investigation.
Normal daily protein excretion should not exceed 150mg/24 hours or
10mg/100mL. Proteinuria is defined by the production of >150mg/day with
nephritic syndrome producing >3.5g/day
Dipstick urinalysis detects protein with Bromphenol blue indicator dye and is
most sensitive to albumin and less sensitive to Bence-Jones protein and
globulins. Trace positive results are equivalent to 10 mg/100 ml or about 150
mg/24 hours (the upper limit of normal).
True protein elevation:
o Renal: Increased renal tubular secretion,increased glomerular
filtration (glomerular disease), nephrotic syndrome,
pyelonephritis, glomerulonephritis, malignant hypertension
o CVS: Benign HT, CCF, SBE
o Functional proteinuria (albuminuria): fever, cold exposure,
stress, pregnancy, eclampsia, CHF, shock, severe exercise
o Other: Orthostatic proteinuria, electric current injury,
hypokalaemia, Cushings syndrome
o Drugs: Aminoglycosides, gold, amphotericin, NSAID,
sulphonamides, penicillins
Note: Bence Jones globulin associated with multiple myeloma, lymphoma and
macroglobulinaemia is NOT detected by dipstick urinalysis
o False Positive: Concentrated urine (UO<2.5L/day), alkaline
urine (pH >7.5), trace residue of bleach, aceazolomide,
cephalosporins, NaHCO3
o False Negative: Dilute urine (UO >5.0 litres/day) or acidic urine
(pH <5)
8. Uji dipstick dan konversinya pada 24-hours urinary excretion
DipstickProtein reading Protein excretion mg/24
hours
Protein excretion
mg/dL
Negative <0.1 <10
Trace 0.1-0.2 15
1+ 0.2-0.5 30
2+ 0.5-1.5 100
3+ 2.0-5.0 300
4+ >5.0 >1000

9. Systemic Lupus Erythematosus Criteria (DOPAMINE RASH)
Discoid rash (erythematous circular raised patches with adherent
keratotic scalling and follicular plugging; atrophic scarring
may occur)
Oral ulcers
Photosensitive
Arthritis (on two or more peripheral joints with tenderness, swelling,
or effusion)
Malar rash
Immune markers (Anti dsDNA, anti-RO, anti-La, anti-Smith)
Neurologic changes (seizure or psychosis without other causes
ESR raised
Renal disease: proteinuria >0.5 g/d or 3+, or cellular cast
ANA +
Serositis (pleurisy, pericarditis)
Hematologic disease (hemolytic anemia, thrombocytopenia,
leukopenia)

10. Perbedaan T3 dan T4:
Perbedaan T3 T4
Sekresi Sangat sedikit disekresi;
sebagian besar
didapatkan oleh
kelenjar tiroid
deiodinisasi peripheral
dari hormone T4
Ketersediaan Serum dalam bentuk berikatan dengan protein
atau free state
Kekuatan ikatan dengan
protein
Lebih lemah sehingga
lebih mudah di uptake
oleh cell
Lebih kuat
Kekuatan ikatan dengan
reseptor nuklear
Lebih cepat Lebih lamban
Keaktifan Lebih aktif secara
biologis
Kurang aktif secara
biologis

Test T4
- Ada 2 bentuk T4 : protein-bounded dan Free T4 (FT4)
- FT4 bentuk aktif yang ada di organ tubuh
- Total T4 normal : 4.5 12.6 g/dL
- Normal FT
4
: 0.7 to 1.8 ng/dL
- Angka total T
4
or FT
4
yang meningkat hyperthyroidism
- Angka total T
4
or FT
4
yang menurun hypothyroidism
- Normal FT4 level disaat total T4 tinggi maupun rendah kesalahan
pada binding protein, bukan pada tiroid.
Contoh : pada masa hamil dan pemakaian oral contraceptives
meningkatkan binding protein
- Penyakit yang berat dan pemakaian kortikosteroid dapat menurunkan
binding protein

Test T3
- Normal FT3 range : 0.2-0.5 ng/dL
- Test T3 tidak berguna dalam mendiagnosis hipotiroid karena hanya
akan turun ketika keadaan sudah sangat parah
- Pada beberapa keadaan FT4 normal tapi FT3 tinggi menggambarkan
hipertiroid


11. Perbedaan C3 & C4 pada pemeriksaan SLE, hasil pemeriksaan dan
interpretasinya
The complement system helps or complements the ability of antibodies
and phagocytic cells to clear pathogens from an organism. It is part of the
immune system called the innate immune system that is not adaptable and
does not change over the course of an individual's lifetime. However, it can be
recruited and brought into action by the adaptive immune system.
The complement system consists of a number of small proteins found in the
blood, in general synthesized by the liver, and normally circulating as inactive
precursors (pro-proteins). When stimulated by one of several triggers,
proteases in the system cleave specific proteins to release cytokines and
initiate an amplifying cascade of further cleavages. The end-result of this
activation cascade is massive amplification of the response and activation of
the cell-killing membrane attack complex. Over 25 proteins and protein
fragments make up the complement system, including serum proteins, serosal
proteins, and cell membrane receptors. They account for about 5% of the
globulin fraction of blood serum.
Three biochemical pathways activate the complement system: the classical
complement pathway, the alternative complement pathway, and the lectin
pathway.
The following are the basic functions of complement:
Opsonization - enhancing phagocytosis of antigens
Chemotaxis - attracting macrophages and neutrophils
Cell Lysis - rupturing membranes of foreign cells
Clumping of antigen-bearing agents
C3 and C4 complement are parts of a group of globulin proteins found in the
blood. Globulins carry substances through the bloodstream. C3 and C4
complement help the body's immune system react to inflammation and
infection.
Laboratory tests which measure complement levels in the blood may also be
helpful to the physician in making a diagnosis of SLE.
Complement is a blood protein that destroys bacteria and also influences
inflammation.
Complement proteins are identified by the letter "C" and a number.
The most common complement tests are C3, C4, and CH50.

If the total blood complement level is low, or the C3 or C4 complement values
are low and the person also has a positive ANA, some weight is added to the
diagnosis of lupus. Low C3 and C4 complement levels in individuals with a
positive ANA may signify the presence of active disease, especially kidney
disease.

12. Indikasi pemberian albumin
Usage Recommended Dosage
ALBUMIN 5%
Hypovolemia Although the volume of ALBUMIN 5% administered must be
individualized, the initial dose should be 250 to 500 mL for older
children and adults and 12 to 20 mL per kg of body weight for
infants and young children. It may be repeated after 30 minute
intervals if the response is not adequate.1

Hemodynamic parameters should be monitored and should be used
to check for risk of hypervolemia and cardiovascular overload.
Hypoalbumine
mia
Hypoalbuminemia is usually accompanied by a hidden extravascular
albumin deficiency of equal magnitude. This total body albumin
deficit must be considered when determining the amount of
albumin necessary to reverse the hypoalbuminemia. When using
patient's serum albumin concentration to estimate the deficit, the
body albumin compartment should be calculated to be 80 to 100
mL per kg of body weight. Daily dose should not exceed 2 g of
albumin per kg of body weight.1
Burns When ALBUMIN 5% is administered after the first 24 hours
following burns, an initial dose of 500 mL is recommended.1

Usage Recommended Dosage
ALBUMIN 25%
Hypovolemic
Shock
The dosage of ALBUMIN 25% must be individualized. As a
guideline, the initial treatment should be in the range of 100 to 200
mL for adults and 2.5 to 5 mL per kg body weight for children. This
may be repeated after 15 to 30 minutes if the response is not
adequate. For patients with significant plasma volume deficits,
albumin replacement is best administered in the form of 5%
Albumin.2

Upon administration of additional albumin or if hemorrhage has
occurred, hemodilution and a relative anemia will follow. This
condition should be controlled by the supplemental administration
of compatible red blood cells or compatible whole blood.2

Hemodynamic parameters should be monitored and should be used
to check for risk of hypervolemia and cardiovascular overload.
Burns The optimal therapeutic regimen for administration of crystalloid
and colloid solutions after extensive burns has not been
established. When ALBUMIN 25% is administered after the first 24
hours following burns, the dose should be determined according to
the patient's condition and response to treatment.2
Hypoalbumine
mia
Hypoalbuminemia is usually accompanied by a hidden extravascular
albumin deficiency of equal magnitude. This total body albumin
deficit must be considered when determining the amount of
albumin necessary to reverse the hypoalbuminemia. When using
patient's serum albumin concentration to estimate the deficit, the
body albumin compartment should be calculated to be 80 to 100
mL per kg of body weight. Daily dose should not exceed 2 g of
albumin per kg of body weight.2
Hemolytic
Disease of the
Newborn
ALBUMIN 25% may be administered prior to or during exchange
transfusion in a dose of 1 g per kg body weight.2